Modulation of calcium channels in human retinal glial cells by basic fibroblast growth factor: a possible role in retinal pathobiology.

The objective of this study was to begin to examine the cellular and biophysical effects on human retinal glial cells of basic fibroblast growth factor (bFGF), which is endogenous to the retina and likely to play a role in retinal pathobiology. Experiments were performed on cultured glial cells derived from the adult postmortem retina. A proliferative response to bFGF established a sensitivity of the retinal glia to this growth factor. The possibility that bFGF alters calcium currents was assessed using the whole-cell recording configuration of the patch-clamp technique to analyze inward currents carried by barium. Two types of voltage-gated calcium channels could be expressed by the glial cells. One, similar to the T-type current described in various kinds of cells, had a low threshold of activation, a transient response, and an insensitivity to the dihydropyridine nifedipine. The other type of inward current, which closely resembles the L-type calcium current found in other cells, had a high threshold, had a long-lasting response, and was inhibited by nifedipine. When continuous whole-cell recordings were made from retinal glial cells, the L-type calcium current increased significantly within 20 min after exposure of the cells to bFGF. The physiological significance of this modulatory effect remains uncertain, though the observation that nifedipine inhibits both the L-type calcium current and the bFGF-induced proliferation is consistent with the hypothesis that dihydropyridine-sensitive channels may play a role in modulating the mitogenic response of retinal glial cells to this growth factor.